RORγt is well recognized as the lineage-defining transcription factor for T helper 17 (T17) cell development. However, the cell-intrinsic mechanisms that negatively regulate T17 cell development and autoimmunity remain poorly understood. Here, we demonstrate that the transcriptional repressor REV-ERBα is exclusively expressed in T17 cells, competes with RORγt for their shared DNA consensus sequence, and negatively regulates T17 cell development via repression of genes traditionally characterized as RORγt dependent, including Il17a. Deletion of REV-ERBα enhanced T17-mediated pro-inflammatory cytokine expression, exacerbating experimental autoimmune encephalomyelitis (EAE) and colitis. Treatment with REV-ERB-specific synthetic ligands, which have similar phenotypic properties as RORγ modulators, suppressed T17 cell development, was effective in colitis intervention studies, and significantly decreased the onset, severity, and relapse rate in several models of EAE without affecting thymic cellularity. Our results establish that REV-ERBα negatively regulates pro-inflammatory T17 responses in vivo and identifies the REV-ERBs as potential targets for the treatment of T17-mediated autoimmune diseases.